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10.1038/srep28565

http://scihub22266oqcxt.onion/10.1038/srep28565
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27349617!4923877!27349617
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suck abstract from ncbi


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pmid27349617      Sci+Rep 2016 ; 6 (ä): 28565
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  • Identification of SLC41A3 as a novel player in magnesium homeostasis #MMPMID27349617
  • de Baaij JH; Arjona FJ; van den Brand M; Lavrijsen M; Lameris AL; Bindels RJ; Hoenderop JG
  • Sci Rep 2016[Jun]; 6 (ä): 28565 PMID27349617show ga
  • Regulation of the body Mg(2+) balance takes place in the distal convoluted tubule (DCT), where transcellular reabsorption determines the final urinary Mg(2+) excretion. The basolateral Mg(2+) extrusion mechanism in the DCT is still unknown, but recent findings suggest that SLC41 proteins contribute to Mg(2+) extrusion. The aim of this study was, therefore, to characterize the functional role of SLC41A3 in Mg(2+) homeostasis using the Slc41a3 knockout (Slc41a3(-/-)) mouse. By quantitative PCR analysis it was shown that Slc41a3 is the only SLC41 isoform with enriched expression in the DCT. Interestingly, serum and urine electrolyte determinations demonstrated that Slc41a3(-/-) mice suffer from hypomagnesemia. The intestinal Mg(2+) absorption capacity was measured using the stable (25)Mg(2+) isotope in mice fed a low Mg(2+) diet. (25)Mg(2+) uptake was similar in wildtype (Slc41a3(+/+)) and Slc41a3(-/-) mice, although Slc41a3(-/-) animals exhibited increased intestinal mRNA expression of Mg(2+) transporters Trpm6 and Slc41a1. Remarkably, some of the Slc41a3(-/-) mice developed severe unilateral hydronephrosis. In conclusion, SLC41A3 was established as a new factor for Mg(2+) handling.
  • |Animals[MESH]
  • |Cation Transport Proteins/genetics/*metabolism[MESH]
  • |Homeostasis/*physiology[MESH]
  • |Hypercalciuria/blood/genetics/urine[MESH]
  • |Magnesium/*blood/*urine[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]
  • |Nephrocalcinosis/blood/genetics/urine[MESH]


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